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Akira Ishiwata

Researcher at Jichi Medical University

Publications -  20
Citations -  788

Akira Ishiwata is an academic researcher from Jichi Medical University. The author has contributed to research in topics: Transplantation & Bone marrow. The author has an hindex of 15, co-authored 19 publications receiving 744 citations. Previous affiliations of Akira Ishiwata include Mitsubishi.

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Severe secondary deficiency of von Willebrand factor-cleaving protease (ADAMTS13) in patients with sepsis-induced disseminated intravascular coagulation: its correlation with development of renal failure.

TL;DR: Deep molecular weight forms of ADAMTS13 were found in the plasma of patients with sepsis-induced DIC, suggesting that the deficiency of ADamTS13 was partially caused by its cleavage by proteases in addition to decreased synthesis in the liver.
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Minimizing the inhibitory effect of neutralizing antibody for efficient gene expression in the liver with adeno-associated virus 8 vectors.

TL;DR: The results suggest that portal vein-directed vector delivery strategies with flushing to remove blood are efficacious for minimizing the inhibitory effect of anti-AAV antibodies.
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Efficient expression of a transgene in platelets using simian immunodeficiency virus-based vector harboring glycoprotein Ibα promoter: in vivo model for platelet-targeting gene therapy

TL;DR: Platelet‐targeting gene therapy using SIV vectors appears to be promising for gene therapy approaches toward not only inherited platelet diseases but also other hemorrhagic disorders such as hemophilia A.
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Liver-restricted expression of the canine factor VIII gene facilitates prevention of inhibitor formation in factor VIII-deficient mice.

TL;DR: Gene therapy for hemophilia A with adeno‐associated virus (AAV) vectors involves difficulties in the efficient expression of factor VIII (FVIII) and in antibody formation against transgene‐derived FVIII.
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Porcine model of hemophilia A.

TL;DR: The data suggest that the hemophilia A pig is a severe hemophile A animal model for studying not only hemophili A gene therapy but also the next generation recombinant coagulation factors, such as recombinant factor VIII variants with a slower clearance rate.